Overexpression of TNF-α converting enzyme promotes adipose tissue inflammation and fibrosis induced by high fat diet

Matsui Yuki; Tomaru Utano; Miyoshi Arina; Ito Tomoki; Fukaya Shinji; Miyoshi Hideaki; Atsumi Tatsuya; Ishizu Akihiro

Title	en Overexpression of TNF-α converting enzyme promotes adipose tissue inflammation and fibrosis induced by high fat diet
Creator	en Matsui, Yuki en Tomaru, Utano NRID 1000020360901 en Miyoshi, Arina en Ito, Tomoki en Fukaya, Shinji en Miyoshi, Hideaki NRID 1000030360902 en Atsumi, Tatsuya NRID 1000020301905 en Ishizu, Akihiro NRID 1000060321957
Accessrights	open access
Subject	Other en Adipose tissue inflammation Other en High fat diet Other en Obesity Other en TACE Other ja TNF-α NDC 491
Description	Abstract en Obesity is a state in which chronic low-grade inflammation persists in adipose tissues. Pro-inflammatory cytokines, including TNF-α, produced by adipose tissues have been implicated as active participants in the development of obesity-related diseases. Since TNF-α converting enzyme (TACE) is the major factor that induces soluble TNF-α, TACE has been noted as a pivotal regulator in this field. To reveal the role of TACE in adipose tissue inflammation, TACE-transgenic (TACE-Tg) and wild type (WT) mice were fed with high fat diet (HFD) or control diet for 16 weeks. At 13 weeks after the beginning of the diet, serum TNF-α and macrophage-related cytokine/chemokine levels were elevated in TACE-Tg mice fed with HFD (Tg-HFD mice), and the number of the so-called crown-like adipocyte was significantly increased in adipose tissues of Tg-HFD mice at the end of the experiment. Although macrophage infiltration was not detected in the adipose tissues at this time, fibrosis was observed around the crown-like adipocytes. These findings suggested that TACE overexpression induced macrophage infiltration and subsequent fibrosis in adipose tissues under HFD regimen. The collective evidence suggested that TACE could be a therapeutic target of HFD-induced obesity-related adipose tissue inflammation.
Publisher	en Elsevier
Date	Issued2014-12
Language	eng
Resource Type	journal article
Version Type	AM
Identifier	HDL http://hdl.handle.net/2115/57002
Relation	isVersionOf DOI https://doi.org/10.1016/j.yexmp.2014.09.017 PMID 25236578
Journal	PISSN 0014-4800 en Experimental and Molecular Pathology Volume Number97 Issue Number3 Page Start354 Page End358
File	fulltext Accepted Manuscript_Matsui et al_Exp Mol Pathol-2.pdf 485.1 KB (application/pdf) Issued2014-12
Oaidate	2023-07-26